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AIR POLLUTION – MONITORING MODELLING AND HEALTH

air pollution – monitoring, modelling and health - Ademloos

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Air Pollution and Cardiovascular Diseases 363<br />

pollution to a larger extent than Western cohorts because they tend to spend more time<br />

outside than indoors while Westerners have more access to air conditioning which tends to<br />

mitigate pollution with the use of filters and recirculated ventilation. In the initial data<br />

published in the PAPA study, Wuhan in mainland China exhibited highest concentrations<br />

of PM10 and O 3 , while Shanghai has the highest concentrations of NO 2 and SO 2 . In<br />

comparison with cities of comparable size in the U.S. (analyzing data from the National<br />

Morbidity and Mortality and Air Pollution Study {NMMAPS}), the concentrations of PM10<br />

and SO 2 were found to be much higher for cities included in the PAPA study. For example,<br />

the concentrations of PM10 in PAPA had means of 52-142 μg/m3 versus 33 μg/m3 in<br />

NMMAPS. In the case of NO 2 and O 3 , the results were similar in that U.S. had lower<br />

concentrations than those in China 38 . When these results were correlated with mortality<br />

figures for cardiovascular and respiratory diseases, predictable patterns emerged. Cause of<br />

death ratios were the highest in Wuhan (4:1), followed by Shanghai (3:1) with lower figures<br />

documented for Bangkok and Hong Kong 38 .<br />

Banerjee et al have recently reported from India that exposure to poor air quality can alter<br />

hematological and immunological parameters negatively. In their study, these investigators<br />

reported results from 2218 individuals residing in the large urban metropolis of New Delhi<br />

ranging in age from 21-65 years who were exposed to vehicular exhaust (the main polluter<br />

of air quality in Asia in general and in India in particular). The authors found the prevalence<br />

of hypertension 4 fold higher than matched controls (Bannerjee M et al, Int J Hyg Environ<br />

Health 2011 Sep 16 Epub). Platelet P-selctins were significantly upregulated in this cohort<br />

while CD4+ T-helper cells and CD19+ B cells were found to be depleted and CD56+ NK<br />

cells were upregulated. These changes in the immune profile is positively correlated with<br />

hypercoagulable states and higher cardiovascular risk 39 . These findings have been<br />

effectively reproduced in other Indian studies as well. For example, Barman and colleagues<br />

have recently published data from Lucknow (a city in Northern India) in which PM and<br />

pollutant heavy metals were also linked to elevated risk of cardiovascular risk 40 . Even<br />

earlier studies have shown strong correlation between air pollution levels and<br />

cardiovascular risk. Nautiyal et al reported in a study completed in the Indian state of<br />

Punjab (a pilot study) demonstrated positive correlations between angina pectoris and<br />

PM10 pollution 41 .<br />

Aside from cardiovascular mortality, other parameters of cardiovascular function have also<br />

been correlated with greater air pollution. For example, in studies from central Europe, a<br />

rise in blood pressure at times of greater air pollution has been reported. In the MONICA<br />

study from Germany, a significant rise in blood pressure was noted in relation with<br />

particulate air pollution even after adjustment for other cardiovascular risk factors 42 .<br />

Significant elevations of diastolic blood pressure in 23 normotensive individuals following<br />

two hours of exposure to PM2.5 were reported by Urch and colleagues 43 . In Brazil,,<br />

monocyte levels also appear to significantly influence systolic, diastolic blood pressure<br />

levels per quartile of monocyte concentration. In this setting, sulfur dioxide levels were also<br />

noted to affect blood pressure, validating the importance of gaseous co-pollutants 44 .<br />

Intriguingly, a large volume of data also suggests that the deleterious effects of particulate<br />

air pollution can be aggravated by the presence of cofactors such as diabetes, obesity,<br />

hypertension, chronic pulmonary disease, and previous cardiovascular disease, as well as an<br />

additive effect of advancing age 45, 46 .

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